Spinal cord injury (SCI) is a severe traumatic disease with high incidence and high disability rate, and repairing the injury always is a difficult problem in international medical community. Due to deficiencies in effective repairing solutions, only less than 1% patients suffered from the SCI have achieved complete recovery of nerve functions.
The spinal cord injuries include primary injuries and secondary injuries. The primary injuries are caused by mechanical compression, bleeding, electrolyte outflow and other factors. The primary spinal cord injuries occur at the moment of being injured, and the injuries are irreversible. However, the scope of the primary injuries is limited. The secondary spinal cord injuries undergo an evolution process that will go on from hours to days and the injuries re reversible. The main injury mechanism of the spinal cord injuries is concerned to secondary injuries after being injured. At present, it has been found that the secondary spinal cord injury process is a complex pathological process in which multiple signaling pathways are involved and a considerable degree of cascade amplifications and cross reactions are present, and thus it has complex regulating mechanisms. Some studies are made to demonstrate that there are complex and diverse factors that will affect regenerations of neurons and axons after injury, including vascular injuries, oxygen free radical release, inflammation over-reaction, electrolyte imbalance (e.g., intracellular calcium overload), and abnormal energy metabolism. Additionally, pathological changes after injury are mainly reflected by changes of microenvironment of the injury site and its surrounding. After spinal cord injury, a series of immunocompetent cells, including neutrophils and activated macrophages, can be recruited around the spinal cord tissues. These cells can produce many pro-inflammatory chemokines/cytokines, such as TNFα, IL-1β, thereby to aggravate the spinal cord injury. In the acute stage, severe inflammatory reactions will result in apoptosis of a large number of cells, which eventually result in formation of local void. In the chronic stage, glial cells migrate into the void and proliferate, to repair the void defect, which results in formation of glial scar. The glial scar hinders the extension of regenerated axons to distal ends, and ultimately, this will seriously affect long-term functional recovery. This change in the pathological environment will largely determine the severity of the final injury, and will greatly influence the repairing effects of interventions. At present, there is no systematic and complete mechanism theory to explain the influences of the pathological environment. Since the exact injury mechanism of the spinal cord injury is not explicit, it is difficult to perform corresponding targeted treatments, and thus the achieved treating effects are not ideal.